The arthritis connection to inflammatory bowel disease (IBD): why has it taken so long to understand it?

The arthritis connection to inflammatory bowel disease (IBD): why has it taken so long to understand it?
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DOI:
10.1136/rmdopen-2020-001558
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发表时间:
2021-04
期刊:
影响因子:
6.2
通讯作者:
Weisman MH
Weisman MH
中科院分区:
医学2区
文献类型:
--
作者:
Ashrafi M;Kuhn KA;Weisman MH

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炎症性肠病(IBD)相关性关节炎是脊椎关节炎(SpA)的一个亚类,100多年来在风湿病学临床和研究界一直缺乏认识。尽管在临床上与类风湿性关节炎和强直性脊柱炎不同,但在上个世纪中期,检测系统取得了进展(类风湿因子,HLA-B27),才令人信服地进行了最终的分离。我们现在知道,相当数量的SpA患者有相关的临床IBD,其中近一半显示亚临床肠道炎症,但肠道和肌肉骨骼系统之间的联系仍然是一个令人烦恼的问题。Nathan Zvaifler的两篇出版物(一个在1960年,另一个在1975年)预见性地描述了肠道和脊柱/外周关节之间的关系,预示着今天世界各地实验室的大部分工作,试图检查连接的基本机制。(很可能有很多)在肠道、环境(大概是我们的肠道植物群)和对肌肉骨骼系统的下游影响之间。已经认识到微生物群系失调沿着微生物群系驱动的T辅助细胞17细胞扩增和免疫细胞迁移至关节的作用,所有这些都发生在人类白细胞抗原系统内外遗传背景的适当背景下。此外,已经注意到介导免疫细胞归巢到肠道和关节的不同粘附分子。本文就IBD-关节炎的起源和演变进行了综述,提出了IBD-关节炎的致病机制和目前需要填补的空白,以全面了解IBD-关节炎。
Inflammatory bowel disease (IBD) associated arthritis is a subgroup of spondyloarthritis (SpA) that has suffered from lack of recognition in rheumatology clinical and research circles for over 100 years. Although clinically distinguishable from rheumatoid arthritis and ankylosing spondylitis, it took advances in detection systems in the middle of the last century (rheumatoid factor, HLA-B27) to convincingly make the final separations. We now know that significant numbers of patients with SpA have associated clinical IBD and almost half of them show subclinical gut inflammation, yet the connection between the gut and the musculoskeletal system has remained a vexing problem. Two publications from Nathan Zvaifler (one in 1960, the other in 1975) presciently described the relationship between the gut and the spine/peripheral joints heralding much of the work present today in laboratories around the world trying to examine basic mechanisms for the connections (there are likely to be many) between the gut, the environment (presumably our intestinal flora) and the downstream effect on the musculoskeletal system. The role of dysregulated microbiome along with microbiome-driven T helper 17 cell expansion and immune cell migration to the joints has been recognised, all of which occur in the appropriate context of genetic background inside and outside of the human leucocyte antigen system. Moreover, different adhesion molecules that mediate immune cells homing to the gut and joints have been noted. In this review, we studied the origins and evolution of IBD-arthritis, proposed pathogenic mechanisms and the current gaps that need to be filled for a complete understanding of IBD-arthritis.
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